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. 2018 Feb 26;9:814. doi: 10.1038/s41467-018-03036-y

Fig. 2.

Fig. 2

Perturbation of glutamine metabolism causes growth defect in embryonic Lkb1 mutant collecting ducts. Live images of E12.5 HoxB7-Cre; RosaTomato (n = 10) (a, b, f, g) and HoxB7-Cre; Lkb1flox/flox; RosaTomato (n = 10) (c, d, h, i) kidneys after 0 (a, f, c, h) or 48 (b, g, d, i) hours of culture in control media (DMEM, ad) or DMEM lacking glutamine (fi). Quantification of the change (Δ) in branch number (number of ureteric bud tips after 48 h—ureteric bud tips at 0 h) for HoxB7-Cre; RosaTomato (e) or HoxB7-Cre; Lkb1flox/flox; RosaTomato (j) kidneys grown in complete DMEM, DMEM-glutamine, DMEM+ 50 µM concentration of the glutaminase inhibitor BPTES, or 1 mM concentration of the Slc1a5 glutamine transporter inhibitor GPNA. n = 10 for each genotype under each condition. Statistical analysis via Mann−Whitney U-test **p < 0.01, ***p < 0.001, ****p < 0.0001, NS not significant. Error bars shown as mean ± standard error of the mean (SEM). Scale bars equal 30 microns